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Core clinical problems > 6c. Fever travel/risks > Flashcards

6c. Fever travel/risks Flashcards

1
Q

History taking ID

A

PC
HoPC
MHx: any autoimmune conditions, cancers, immunodeficiency
DHx: immunosuppressants, neutropenia causing drugs
FHx: Is anyone in the family ill?
SHx: travel, sexual contact, intravenous drugs, food, occupation, pets, hobbies
ICE:

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2
Q

Examination ID

A
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3
Q

How to ask about sexual contact

A

I’m trying to assess where this fever is coming from and one of the things I need to think about is infections that can be picked up from sexual activity. Is it okay if I ask you a few questions about your sexual activity? Please feel free to decline answering any of my questions.
Are you sexually active?
When was the last time you were sexually active?
Is that a regular partner or a new partner?
Was it a man or a woman?
Was it oral, vaginal or anal sex?
(Were you giving or receiving in the anal sex?)
Have you ever participated in ‘chemsex’ ?
Have you ever engaged with sex work?
Before this encounter, have you been sexually active with anyone else in the past 6 months?

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4
Q

buffer

A
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5
Q

buffer

A
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6
Q

buffer

A
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7
Q

buffer

A
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8
Q

causes hepatitis

A

alcoholic hepatitis
non alcoholic fatty liver disease
viral hepatitis
autoimmune hepatitis
drug induced hepatitis

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9
Q

Presentation hepatitis

A

abdominal pain, fatigue, pruritus, muscle and joint aches, N+V, jaundice, fever (viral hepatitis)

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10
Q

LFTs and bilirubin in hepatitis

A

LFTS: “hepatitic picture” - high transaminases (AST/ALT) with proportionally less of a rise in ALP.

Transaminases are liver enzymes released into the blood as a result on inflammation of the liver cells
Bilirubin can also rise as a result of inflammation of the liver cells—> jaundice

Elevation in unconjugated bilirubin indicates pre-hepatic or hepatic jaundice eg hepatitis. Whereas conjugated indicates he pato cellular or cholestasis.

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11
Q

viral hepatitis mneumonic

A

A - ass (F-O)
B - blood-borne (PP)
C - cerious and circulation (PP)
D - depends on B (PP)
E - eating (F-O)

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12
Q

why is the liver scanned in hepatitis, what are you looking for?

A

Cirrhosis : fibroscan
Hepatocellular carcinoma : USS

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13
Q

initial testing for hepatitis B

A

Surface antigen (HBsAg) – active infection
Core antibodies (HBcAb) – implies past (or current) infection

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14
Q

Which viral hepatitis is a DNA virus

A

hepatitis B

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15
Q

HBsAG

A

hep B surface antigen

= active infection /chronic infection

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16
Q

HBsAb

A

hep B surface antibody

= immunised
= infection cleared after exposure
= current infection

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17
Q

HBcAb

A

core antibodies

= past infection cleared after exposure
= chronic infection

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18
Q

E antigen (HBeAg)

A

marker of viral replication and implies high infectivity

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19
Q

E antibody

A

evidence of immune response

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20
Q

Hepatitis B virus DNA (HBV DNA)

A

this is a direct count of the viral load

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21
Q

what are the treatments for hep B

A
  1. Pegylated Interferon alpha (weekly injectable for 48 weeks) which aims to stimulate the immune system to fight the virus,
  2. oral anti-viral agent which suppresses viral replication (Tenofovir or Entecavir once a day, long term)
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22
Q

lifestyle advice to reduce infecting others at hep B diagnosis

A
  • Avoid having unprotected sex, unless the partner has been vaccinated and is immune
  • Avoid sharing needles in inject drugs
  • Avoid sharing toothbrushes or razors with people in the house
  • Avoid drinking alcohol
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23
Q

Hep B summary

A

Type: DNA virus
Transmission: Blood or bodily fluids (sexual intercourse, sharing needles, tattoos, toothbrushes, surgical procedures, vertical transmission)
Vaccine available: yes

Acute infection self resolves in 90% of patients, 10% become chronic as it integrates DNA into own DNA so carrier continues to produce viral proteins

Not curable but can use pegylated interferon alpha or oral anti-virals such as tenofovir or entecavir to keep virus at bay if it is affecting the liver

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24
Q

what is main risk factor for hep C

A

IVDU

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25
Q

invetsigation hep C

A

Hepatitis C antibody test: will be positive if the patient has ever been exposed to the hepatitis C virus, but DOESN’T mean they are actively infected

HCV RNA is done in patients with a positive HCV antibody to confirm current infection, by means of a PCR.

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26
Q

normal course of hep C?

A

1/4 self resolve, rest chronic hep C

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27
Q

what is aim of hep C tretament

A

cure

All patients with current HCV infection (HCV RNA detected) should be offered a course of potentially curative treatment.
Cure is defined as an undetectable HCV RNA in blood 12 weeks after the end of treatment (sustained virological response – “SVR12”).

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28
Q

what drugs are used to treat hep C

A
  1. NS3/4A protease inhibitors (end in –previr) e.g. grazoprevir
  2. NS5A inhibitors (end in –asvir) e.g. elbasvir
  3. NS5B inhibitors (end in –buvir) e.g. sofosbuvir
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29
Q

side effects interferon alpha

A

flu-like symptoms, depression, fatigue, leukopenia, thrombocytopenia

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30
Q

complications of chronic hep C

A

rheumatological problems: arthralgia, arthritis
eye problems: Sjogren’s syndrome

cirrhosis (5-20% of those with chronic disease)
hepatocellular cancer

cryoglobulinaemia: typically type II (mixed monoclonal and polyclonal)

porphyria cutanea tarda (PCT): it is increasingly recognised that PCT may develop in patients with hepatitis C, especially if there are other factors such as alcohol abuse

membranoproliferative glomerulonephritis

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31
Q

hep C summary

A

Type: RNA virus
Transmission: blood and bodily fluids, At risk groups include intravenous drug users and patients who received a blood transfusion prior to 1991 (e.g. haemophiliacs).
Vaccine available: no
test: hep C antibody test- if positive test for RNA to confirm current infection

treatment:
antiviral medication for 8-12 weeks (curative in 90% of patients) grazoprevir, elbasvir, sofobuvir

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32
Q

summary hep D

A

Type: RNA virus
Occurs only in people with hepatitis B infection (attaches to HBsAg)
Increases complications and severity of Hep B
Notifiable disease
test: PCR of hep D RNA

no treatment, inteferon sometimes used but poor evidence

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33
Q

what is hepB/hepD co-infection vs superinfection

A

Co-infection: Hepatitis B and Hepatitis D infection at the same time.
Superinfection: A hepatitis B surface antigen positive patient subsequently develops a hepatitis D infection.

Superinfection is associated with high risk of fulminant hepatitis, chronic hepatitis status and cirrhosis.

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34
Q

what is fulminant hepatitis

A
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35
Q

What is AIDS usually referred to in the UK

A

late stage HIV

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36
Q

most common type of HIV?

A

HIV-1

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37
Q

natural history of HIV

A

An initial seroconversion flu-like illness occurs within a few weeks of infection.

The infection is then asymptomatic until it progresses and the patient becomes immunocompromised and develops AIDS-defining illnesses and opportunistic infections potentially years later.

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38
Q

typical history HIV seroconversion?

A

typically presents as a glandular fever type illness. Increased symptomatic severity is associated with poorer long term prognosis. It typically occurs 3-12 weeks after infection

Features
sore throat
lymphadenopathy
malaise, myalgia, arthralgia
diarrhoea
maculopapular rash
mouth ulcers
rarely meningoencephalitis

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39
Q

How is HIV spread?

A

Unprotected anal, vaginal or oral sexual activity.

Mother to child at any stage of pregnancy, birth or breastfeeding. This is referred to as vertical transmission.

Mucous membrane, blood or open wound exposure to infected blood or bodily fluids such as through sharing needles, needle-stick injuries or blood splashed in an eye.

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40
Q

what is the standard testing for HIV

A

combined (HIV antibody and HIV p24 antigen)
- if positive repeat to confirm
- if negative, repeat in 3 months

If exposure test:
- 4 weeks after exposure and 3 months

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41
Q

what is normal CD4 count

A

500-1200 cells/mm3

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42
Q

what CD4 count is considered end-stage HIV

A

under 200 cells/mm3

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43
Q

What does “undetectable” refer to?

A

Viral load is the number of copies of HIV RNA per ml of blood.

“Undetectable” refers to a viral load below the labs recordable range (usually 50 – 100 copies/ml).

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44
Q

Standard treatment HIV?

A

2 Nucleoside Reverse Transcriptase Inhibitors (NRTIs) - eg tenofovir and emtrictiabine

PLUS a third agent

Often: Integrase inhibitor eg doultegrovir

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45
Q

what prophylaxis is given to patients with a CD4 count <200

A

Prophylactic co-trimoxazole (Septrin) is given to patients with CD4 < 200/mm3 to protect against pneumocystis jirovecii pneumonia (PCP).

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46
Q

What monitoring do pts with HIV need?

A
  • viral load
  • CD4 count
  • HIV have close monitoring of cardiovascular risk factors and blood lipids and appropriate treatment (such as statins) to reduce their risk of developing cardiovascular disease.
  • Yearly cervical smears are required for women. HIV predisposes to developing cervical human papillomavirus (HPV) infection
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47
Q

What vaccines are ppl with HIV offered?

A

annual influenza, pneumococcal (every 5-10 years), hepatitis A and B, tetanus, diphtheria and polio.

Patients should avoid live vaccines.

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48
Q

Advice for sexual activity HIV

A

Advise condoms for vaginal and anal sex and dams for oral sex even with when both partners are positive.

If the viral load is undetectable then transmission through unprotected sex is unheard of in large studies but not impossible.

Partners should have regular HIV tests.

Where the affected partner has an undetectable viral load unprotected sex and pregnancy may be considered.

It is also possible to conceive safely through techniques like sperm washing and IVF.

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49
Q

What is standard risk of HIV vertical transmission

A

25-30%

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50
Q

What factors reduce risk of vertical transmission HIV

A

Factors which reduce vertical transmission (from 25-30% to 2%)

maternal antiretroviral therapy
mode of delivery (caesarean section)
neonatal antiretroviral therapy
infant feeding (bottle feeding)

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51
Q

when can vaginal delivery be considered for pts with HIV

A

vaginal delivery is recommended if viral load is less than 50 copies/ml at 36 weeks

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52
Q

standard management of birth HIV

A

caesarian section is recommended

a zidovudine infusion should be started four hours before beginning the caesarean section

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53
Q

How should a neonate born to a HIV positive mother be managed

A

zidovudine is usually administered orally to the neonate if maternal viral load is <50 copies/ml.

Otherwise triple ART should be used.

Therapy should be continued for 4-6 weeks.

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54
Q

can you breastfeed HIV

A

No

Not recommended

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55
Q

Post exposure prophylaxis HIV

A

HIV tests should be done initially but also a minimum of 3 months after exposure to confirm a negative status.

Truvada (emtricitabine / tenofovir) and raltegravir for 28 days.

Start within 1-2 hours - may be started up to 72 hours

Individuals should abstain from unprotected activity for a minimum of 3 months until confirmed negative.

see the BHIVA link for charts which outline the risk depending on the incident. Generally, low-risk incidents such as human bites don’t require post-exposure prophylaxis

reduces risk of transmission by 80%

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56
Q

What opportunistic conditions may present CD4 200-500

A

oral thrush
shingles
hairy leukoplakia
kaposi sarcoma

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57
Q

what is kaposi sarcoma caused by

A

HHV-8 (human herpes virus 8)

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58
Q

Presentation kaposi sarcoma? management?

A

purple papules or plaques on the skin or mucosa (e.g. gastrointestinal and respiratory tract)
skin lesions may later ulcerate
respiratory involvement may cause massive haemoptysis and pleural effusion

radiotherapy + resection

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59
Q

what opportunistic conditions may develop CD4 100-200

A

cryptosporidiosis
cerebral toxoplasmosis
Pneumocystis jirovecii pneumonia

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60
Q

what is cryptosporidiosis

A

commonest protozoal cause of diarrhoea in the UK. Two species, Cryptosporidium hominis and Cryptosporidium parvum account for the majority cases.

Cryptosporidiosis is more common in immunocompromised patients (e.g. HIV) and young children.

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61
Q

features cryptosporidiosis

A

watery diarrhoea
abdominal cramps
fever

in immunocompromised patients, the entire gastrointestinal tract may be affected resulting in complications such as sclerosing cholangitis and pancreatitis

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62
Q

diagnosis cryptosporidiosis

A

stool: modified Ziehl-Neelsen stain (acid-fast stain) of the stool may reveal the characteristic red cysts of Cryptosporidium

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63
Q

management cryptosporiiosis

A

immunocompetent - supportive

HIV - start antiretroviral therapy - usually resolves crypto

nitazoxanide , rifaximin

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64
Q

what is toxoplasmosis

A

Toxoplasma gondii is an obligate intracellular protozoan that infects the body via the gastrointestinal tract, lung or broken skin. It’s oocysts release trophozoites which migrate widely around the body including to the eye, brain and muscle. The usual animal reservoir is the cat, although other animals such as rats carry the disease.

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65
Q

How does toxoplasmosis affect immunocompetent patients?

A

Most infections are asymptomatic. Symptomatic patients usually have a self-limiting infection, often having clinical features resembling infectious mononucleosis (fever, malaise, lymphadenopathy). Other less common manifestations include meningoencephalitis and myocarditis.

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66
Q

How does toxoplasmosis affect immunosuppressed?HIV patients. management?

A

Cerebral toxoplasmosis accounts for around 50% of cerebral lesions in patients with HIV

constitutional symptoms, headache, confusion, drowsiness

CT: usually single or multiple ring-enhancing lesions, mass effect may be seen

management: pyrimethamine plus sulphadiazine for at least 6 weeks

Immunosuppressed patients may also develop a chorioretinitis secondary to toxoplasmosis.

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67
Q

opportunistic conditions CD4 50-100

A

Aspergillosis
oesophageal candidiasis
Cryptococcal meningitis (fungal)
primary CNS lymphoma secondary to EBV

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68
Q

ddx focal neurological lesion HIV

A

toxoplasmosis 50%
primary CNS lymphoma 30%

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69
Q

how to differentiate between toxoplasmosis and priamry CNS lymphoma in patients with HIV focal neuro

A

toxo:
Multiple lesions
Ring or nodular enhancement
Thallium SPECT negative

lymphoma:
Single lesion
Solid (homogenous) enhancement
Thallium SPECT positive

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70
Q

managment priamry CNS lymphoma

A

Steroids (may significantly reduce tumour size)

Chemotherapy (e.g. methotrexate) + with or without whole brain irradiation.

Surgical may be considered for lower grade tumours

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71
Q

opportunistic condition CD4 <50

A

cytomegalovirus retinitis

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72
Q

presentation CMV retinitis? management?

A

visual impairment e.g. ‘blurred vision’. Fundoscopy shows retinal haemorrhages and necrosis, often called ‘pizza’ retina

IV ganciclovir

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73
Q

encephalitis HIV patients causes

A

may be due to CMV or HIV itself
HSV encephalitis but is relatively rare in the context of HIV
CT: oedematous brain

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74
Q

characteristic feature of CMV infected cells

A

infected cells have a ‘Owl’s eye’ appearance due to intranuclear inclusion bodies

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75
Q

How does CMV affect immunocompetent patients

A

usually asymptomatic

can cause mononucelosis type illness

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76
Q

what is gastroenteritis

A

Gastroenteritis is a transient disorder due to enteric infection, usually caused by viruses, characterised by sudden onset of diarrhoea, with or without vomiting.

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77
Q

what is dysentery

A

Dysentery is an infection of the intestines that causes diarrhoea containing blood or mucus.

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78
Q

define acute diarrhoea

A

3 or more episodes of liquid or semi-liquid stool in a 24-hour period,

lasting for less than 14 days, where the stool takes the shape of the sample pot.

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79
Q

define prolonged diarrhoea

A

acute-onset diarrhoea that has persisted for over 14 days.

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80
Q

complications of gastroenteritis

A

dehydration, electrolyte disturbance, acute kidney injury, sepsis, haemolytic uraemic syndrome, and secondary irritable syndrome or inflammatory bowel syndrome.

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81
Q

Approach to gastroenteritis

A

Assess for signs of dehydration, sepsis, shock (SEE DEHYDRATION AND SHOCK)

  1. Arrange hospital admission if sys unwell/sepsis/severe dehydration/child with ? or confirmed STEC/?HUS
  2. Arrange for stool culture and sensitivity if indicated
    sys unwell/dysentry/recent abx or PPI (to exclude c.diff)/diarrhoea not resolved by day 7/?food poisoning/recent travel/someone at risk of transmission/asymp been in contact with risky contacts eg confirmed STEC or giardia
  3. Send additional 3 samples 2-3 days apart for ova, cysts and parasites if recent travel or symptoms >14 days
  4. Hydration, ORS if at risk
  5. advise abx or antimotility or antiemetics and probiotics not routinely reccomended
  6. Advise measures to prevent transmission eg hygeine, 60 degrees, 48 hours symptom free before return to work
  7. Notify PH fir food poisoning, HUS, infectious bloody diarrhoea, enteric fever, cholera
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82
Q

most common cause gastroenteritis

A

viral

rotavirus in children (immunnity long lasting)

norovirus in adults (immunity short lasting)

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83
Q

typical history norovirus

A

Sudden-onset nausea is followed by projectile vomiting and watery diarrhoea. There may be associated fever, headache, abdominal pain, and myalgia.

Most people make a full recovery within 1–2 days.

Symptoms begin 24–48 hours after infection and last for 12–60 hours.

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84
Q

causes of travellers diarrhoea

A

e.coli most common

campylobacter jej

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85
Q

gastroenteritis causes incubation period 1-6 hrs

A

staph aureus
bacillus cereus

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86
Q

gastroenteritis causes incubation period 12-48 hrs

A

salmonella
e.coli

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87
Q

gastroenteritis causes incubation period 48-72 hours

A

shigella
camylobacter

88
Q

gastroenteritis causes incubation period >7days

A

giardiasis
amobiasis

89
Q

what gastroenteritises may cause dysentery

A

e.coli 0157
shigella
amobieasis

90
Q

management campylobacter jejuni

A

almost always supportive

however if symptoms are severe (high fever, bloody and/or high-output diarrhoea) or the person is immunocompromised, consider early prescribing with clarithromycin 250–500 mg twice daily for 5–7 days, within 3 days of onset of illness

91
Q

management e.coli

A

Illness is usually self-limiting and resolves within 10 days

seek specialist advice for:
- whether stool testing for clearance is required
- monitoring for HUS

92
Q

typical history staph aureus gastroenteritis

A

Short incubation period eg 6 hours, severe vomiting

93
Q

typical history bacillus cereus

A

vomiting within 6 hours, stereotypically due to rice

diarrhoeal illness occurring after 6 hours

94
Q

typical history campylobacter jejuni

A

PC: abdo cramps, diarrhoea often with blood, vomiting, fever, flu-like prodrome
Incubation 2-5 days, symptoms resolve after 3-6 days
Risk factors: travel, undercooked meat (particularly poultry), unpasteurised milk, untreated water. Source often not found

95
Q

what type of pathogen is e.coli, gram etc

A

facultative anaerobic, lactose-fermenting, Gram negative bacilli

96
Q

typical history e.coli

A

PC: Watery stools with or without blood, abdominal cramps, nausea, fever.
Illness is usually self-limiting and resolves within 10 days.

Risk factors: travel, contact with faeces, unwashed salad, contaminated meat

97
Q

typical history salmonella

A

PC: watery and sometimes bloody diarrhoea, abdominal pain, headache, nausea, vomiting, and fever. The illness usually lasts for 4–7 days, and people usually recover spontaneously.

The majority of cases are sporadic, but outbreaks may occur in the general population and in institutions.

Ingestion of contaminated food is the most common source, such as red and white meats, raw eggs, milk, and dairy products. Person-to-person spread and contact with infected animals can also occur.

98
Q

typical history shigella

A

Typically, 1–3 days after infection, there is diarrhoea (may have blood and mucus), fever, and abdominal cramps, with or without nausea and vomiting, headache, and malaise. Shigellosis usually resolves in 5–7 days.

99
Q

management shigella

A

Antibiotic treatment is not usually needed for people with mild symptoms.
If symptoms are severe (high fever, bloody and/or high-output diarrhoea) or the person is immunocompromised, seek specialist advice on the need for antibiotic treatment.

100
Q

typical history yersinia enterocolitica

A

rare infection and occurs most commonly in children.
PC: watery diarrhoea (which is often bloody), fever, and abdominal pain. In older children and adults, right-sided abdominal pain and fever may occur.
Symptoms typically develop 4–7 days after exposure and may last 2 days to 6 weeks.

Y. enterocolitica is transmitted by direct contact with infected animals and person-to-person (faecal-oral route), and through contaminated food (especially raw pork and pork products) and water.

101
Q

typical history cryptosporidiosis

A

PC: profuse watery diarrhoea associated with abdominal cramps or pain, nausea, vomiting, fever, and loss of appetite. Symptoms usually last for 1–2 weeks, and recurrence of symptoms is reported in around one-third of cases.

risk: recent travel, water, food

102
Q

typical history amoebiasis

A

PC: mild diarrhoea and abdominal pain, but severe disease (amoebic dysentery) can occur, causing fever, severe abdominal pain, and blood and mucus in the faeces.

103
Q

management amoebiasis

A

Drug treatment is usually recommended for all confirmed cases after specialist advice, such as metronidazole followed by the anti-protozoal drug diloxanide. (to eliminate intraluminal cysts)

Seek specialist advice regarding the need for microbiological clearance to confirm treatment success, 1 week after completing treatment.

104
Q

complication of amoebic gastroenteritis? management?

A

Amoebic liver abscess

usually a single mass in the right lobe (may be multiple). The contents are often described as ‘anchovy sauce’

features
fever
right upper quadrant pain
systemic symptoms e.g. malaise
hepatomegaly

investigations
ultrasound
serology is positive in > 95%

management
oral metronidazole
a ‘luminal agent’ (to eliminate intraluminal cysts) is recommended usually as well e.g. diloxanide furoate

105
Q

typical history giardia

A

prolonged diarrhoea, malaise, abdominal pain, loss of appetite, flatulence, bloating, and rarely nausea. Malabsorption, weight loss, and faltering growth may occur in children

106
Q

management giardia

A

tinidazole 2 g as a single dose

107
Q

Complication of e.coli and shigella

A

haemolytic uraemic syndrome?

108
Q

typical history HUS? triad?

A

PC: brief gastroenteritis, bloody diarrhoea. 5 days after : decreased urine output, hematuria, abdo pain, lethargy, bruising, hematuria, confusion, hypertension

Triad: haemolytic anaemia, acute kidney injury, thrombocytopenia

109
Q

why are antibiotics and antimotility agents not recommended in gastroenteritis

A

if has shiga toxin producing pathogen –> increases risk of HUS

110
Q

management HUS

A

HUS is a medical emergency and has up to 10% mortality
Supportive
Antihypertensives
Blood transfusion
Hemodialysis

111
Q

What respiratory infection should you consider in immunocompromised patients

A

Aspergillus = fungus
Aspergillosis is an infection caused by the fungus aspergillus
Aspergillioma = aspergillus growing in a cavity often created by a previous condition

112
Q

risk factors for invasive aspergillosis

A

Risk factors include:
HIV
Leukaemia
Following broad-spectrum antibiotics

113
Q

presentation aspergilloma

A

Usually asymptomatic but features may include
cough
haemoptysis (may be severe)

114
Q

presentation cholera

A

profuse ‘rice water’ diarrhoea, dehydration, hypoglycaemia

115
Q

MAnagement of cholera

A

oral rehydration therapy,

antibiotics: doxycycline, ciprofloxacin

116
Q

management aspergillosis

A

voriconazole

117
Q

When should you suspect malaria?

A

Suspect malaria in anyone who has returned from or previously visited an area endemic for malaria, who is unwell, or has a fever or history of fever, regardless of malaria chemoprophylaxis.

118
Q

How long after infection does malaria present?

A

Almost all cases of P. falciparum malaria present within 6 months of exposure and most within 2–3 months.

Infection with other malaria species, such as P. ovale and P. vivax may present months or years after exposure due to reactivation of hypnozoites (a dormant liver stage).

Presentation may be delayed in people who have taken chemoprophylaxis.

119
Q

Life cycle of malaria parasite?

A

Malaria is caused by parasites from the plasmodium species.
These parasites are carried by female anopheles mosquitoes and are passed onto humans when they bite.
Once the parasites enter the bloodstream, they travel to the liver where they replicate within hepatocytes → these are then released into the circulation and infect red blood cells.
The parasites replicate within the RBC and feed on the haemoglobin within red blood cells → ruptures RBC → infect more RBC and the cycle continues.

120
Q

Pathophysiology malaria

A

The parasites replicate within the RBC and feed on the haemoglobin within red blood cells → ruptures RBC → infect more RBC and the cycle continues

The rupture of RBC leads to anaemia (haemolytic anaemia) → jaundice, splenomegaly

There is also an innate immune response which leads to symptoms such as fever, chills, rigors, headache, arthralgias, myalgia

Severe malaria can develop when malaria goes untreated, and is much more likely with plasmodium falciparum

P.falciparum causes sequestration whereby RBC clump to endothelial cells → this can impair blood flow → ischaemic damage to organs → organ failure (which is worsened by haemolytic anaemia)

anaemia + sequestration –> ischaemia + organ failure

121
Q

Man returns from trip abroad with maculopapular rash and flu-like illness

A

think HIV seroconversion

122
Q

Returning traveller with fever, RUQ pain →

A

? amoebic liver abscess

123
Q

Fever, abdominal pain, constipation, blanching erythematous rash

A

Typhoid

124
Q

why is p.falciparum the most severe type of malaria?

A

P.falciparum causes sequestration whereby RBC clump to endothelial cells → this can impair blood flow → ischaemic damage to organs → organ failure (which is worsened by haemolytic anaemia)

125
Q

why is there a cyclical nature to fevers in malaria?

A

The time from infecting the RBC to bursting takes some time and when they burst there is an immune response which causes fever - this means there is a cyclical nature to the fevers eg every 24 hours/every 48 hours.

126
Q

what symptoms may indicate severe malaria

A

Impaired consciousness
Extreme weakness
Convulsions
Acidosis (may cause hyperventilation)
Hypoglycaemia
Severe anaemia
Renal impairment
Jaundice
Pulmonary oedema
Significant bleeding
Shock
Hyperparasitaemia

127
Q

gold standard test malaria

A

blood film

128
Q

what is the benefit of thick and thin blood films in malaria diagnisis

A

thick: more sensitive
thin: determine species

129
Q

Investigations malaria

A

RDTs (rapid diagnostic tests)
Blood film (GOLD STANDARD)

130
Q

fbc malaria

A

thrombocythaemia is characteristic
normochromic normocytic anaemia
normal white cell count
reticulocytosis

131
Q

management malaria

A

refer to guidelines

severe
1. artesunate

uncomplicated
1. arteminisin combination therapy eg artesunate + amodiaquine (ACT)

132
Q

of the people exposed to TB, how many will develop it in their lifetime

A

5% get latent TB which becomes active a long time after infection

5% get active TB within 2 years

133
Q

Typical history TB

A

Tuberculosis usually presents with a history of chronic, gradually worsening symptoms. Most cases are of pulmonary TB (around 70%) but they often have systemic symptoms.

Typical signs and symptoms of TB include:
Lethargy
Fever or night sweats
Weight loss
Cough with or without haemoptysis
Lymphadenopathy
Erythema nodosum
Spinal pain in spinal TB (also known as Pott’s disease of the spine)

134
Q

what is the mantoux test for TB?

A

mantoux test - tuberculin skin prick - 5mm or more = positive

Positive in previous vaccination, latent TB or actvive TB

135
Q

what is the quatiferon test for TB?

A

Interferon-Gamma Release Assays (IGRAs)
This test involves taking a sample of blood and mixing it with antigens from the TB bacteria. In a person that has had previous contact with TB the white blood cells have become sensitised to those antigens and they will release interferon-gamma as part of an immune response. If interferon-gamma is released from the white blood cells then this is considered a positive result.

positive in latent TB and active TB

think about pre-test probability before ordering this test

136
Q

what is the gold standard invetsigation for active TB

A

Sputum culture.

Once cultured you can stain it (in same way as a smear) - more likely to be positive as has time to grow

more sensitive than a sputum smear and nucleic acid amplification tests
can assess drug sensitivities
can take 1-3 weeks (if using liquid media, longer if solid media)

If they are not producing sputum then hypertonic saline can be used to induce sputum that can be collected. They might require bronchoscopy with lavage to collect sputum samples.

Other cultures:
Mycobacterium blood cultures. These require special blood culture bottle.
Lymph node aspiration or biopsy

137
Q

what is a sputum smear TB? results?

A

It is where a sputum sample is stained wither using ziel-neelson or phenoralamine - immunofluoresence test

3 specimens are needed
rapid and inexpensive test

stained for the presence of acid-fast bacilli (Ziehl-Neelsen stain)

all mycobacteria will stain positive (i.e. nontuberculous mycobacteria)

the sensitivity is between 50-80%
this is decreased in individuals with HIV to around 20-30%

138
Q

what is a NAAT/PCR for TB?

A

allows rapid diagnosis (within 24-48 hours)

more sensitive than smear but less sensitive than culture

It provides information about the bacteria faster than a traditional culture but is only used where having this information would affect treatment or they are at higher risk of developing complications (i.e. in HIV).

139
Q

how does primary TB present on CXR

A

patchy consolidation, pleural effusions and hilar lymphadenopathy

apical consolidation (top of lungs)

Development of tuberculous pleural effusion may occur as a result of delayed hypersensitivity reaction to mycobacteria or mycobacterial antigens in the pleural space in sensitized individuals [10] or by rupture of a subpleural focus of pulmonary disease into the pleural space

140
Q

how does reactivated TB appear on CXR

A

upper lobe cavitation (gas filled spaces in the lungs) typically in the upper zones

141
Q

how does miliary TB show on CXR

A

“millet seeds” uniformly distributed throughout the lung fields

142
Q

most common site for TB infection?

A

lungs as get plenty O2

143
Q

how may lymph node TB present

A

cold abscess” is a firm painless abscess caused by TB, usually in the neck. They do not have the inflammation, redness and pain you would expect from an acutely infected abscess.

144
Q

where may you get granulomas TB

A

Pulmonary

Extrapulmonary:
lymph nodes
Pleura
Central nervous system
Pericardium
Gastrointestinal system
Genitourinary system
Bones and joints
Cutaneous TB affecting the skin

145
Q

what is miliary TB

A

the immune system is unable to control the disease this causes a disseminated, severe disease

146
Q

what type of vaccine is BCG

A

intradermal injection of live attenuated (weakened) TB

147
Q

what must you do before BCG vaccine?

A

Prior to the vaccine patients are tested with the Mantoux test and given the vaccine only if this test is negative. They are also assessed for the possibility of immunosuppression and HIV due to the risks related to a live vaccine.

148
Q

who is eligible for BCG vaccine?

A

Neonates born in areas of the UK with high rates of TB
Neonates with relatives from countries with a high rate of TB
Neonates with a family history of TB
Unvaccinated older children and young adults (< 35) who have close contact with TB
Unvaccinated children or young adults that recently arrived from a country with a high rate of TB
Healthcare workers

149
Q

management latent TB

A

Otherwise healthy patients do not necessarily need treatment for latent TB. Patients at risk of reactivation of latent TB can be treated with either:

Isoniazid (with pyridoxine) and rifampicin for 3 months
(good for ppl under 35 if hepatotoxcity is a concern)

Isoniazid (with pyridoxine) for 6 months
(for ppl where rifampicin is a concern eg HIV or post transplant)

150
Q

Management of active TB?

A

combination of 4 drugs used at the same time:

R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months

151
Q

they are started on RIPE, what else should be prescribed?

A

pyridoxine (vitamin B6) is usually co-prescribed prophylactically to help prevent peripheral neuropathy from isoniazid

152
Q

MoA and side effects rifampicin

A

“red and orange pissin”
hepatitis, organe secretions

inhibits bacterial DNA dependent RNA polymerase preventing transcription of DNA into mRNA

153
Q

MoA and side effects isoniazid?

A

“Im-so-numb-i-said”
peripheral neuropathy
hepatitis, orange secretions
agranulocytosis

inhibits mycolic acid synthesis

154
Q

MoA and side effects pyrazinamide

A

hyperuricarmia causing gout
arhtalgia, myalgia
hepatitis

converted by pyrazinamidase into pyrazinoic acid which in turn inhibits fatty acid synthase (FAS) I

155
Q

MoA and side effects ethambutol?

other consideration

A

“eye-thambutol”
optic neuritis: check visual acuity before and during treatment

dose needs adjusting in patients with renal impairment

inhibits the enzyme arabinosyl transferase which polymerizes arabinose into arabinan

156
Q

which TB medications can cause hepatitis? how does it present?

A

RIP
- rifampicin
- isoniazid
- pyrazinamide

Abdominal pain, nausea, vomiting, unexplained fatigue or jaundice - stop taking and test liver function

157
Q

microorganism diptheria

A

Corynebacterium diphtheriae

Gram positive bacteria

158
Q

What is diptheria? how does it present?

A

Diphtheria toxin commonly causes a ‘diphtheric membrane’ on tonsils caused by necrotic mucosal cells. Systemic distribution may produce necrosis of myocardial, neural and renal tissue

Possible presentations
recent visitors to Eastern Europe/Russia/Asia
sore throat with a ‘diphtheric membrane’ - grey, pseudomembrane on the posterior pharyngeal wall
bulky cervical lymphadenopathy
may result in a ‘bull neck’ appearanace
neuritis e.g. cranial nerves
heart block

159
Q

Plan ?diptheria

A

Investigations
culture of throat swab: uses tellurite agar or Loeffler’s media

Management
intramuscular penicillin
diphtheria antitoxin

160
Q

when should you suspect viral hemorrhagic fever?

A

VHF should be on the differential diagnosis of travellers with unexplained pyrexia returning from an affected area.

It should rise very high on the list of differential diagnosis if there are features suggesting
bleeding
hypovolaemia
increased vascular permeability
organ failure.
Suspected VHF is a medical and public health emergency and immediate advice should be sought from the local Communicable Disease Consultant on how to proceed[1] .

161
Q

what types of virus are viral haemorrhagic fevers caused by?

A

RNA viruses

162
Q

general disease course VHF

A
  1. Incubation 2-21 days
  2. Viremia affecting the vascular system : flushing, conjunctival injection, petechia haemorrhage, fever, myalgia
  3. Increased vascular permeability: mucous membrane haemorrhage, hypovolemia, hypotension, shock and cirucaltory collapse
    - Direct organ damage may be caused by the viruses themselves; multiorgan damage may also result from shock and hypovolaemia.
    - Different VHFs vary in their infectivity, virulence and tendency to affect specific sites such as liver, brain, kidney and lungs.
163
Q

what specific things should you ask about ?VHF

A

There may be a history of foreign travel, or of recent contact with someone who has become unwell.

Remembered exposure to rodents, bats and insect bites may be significant, as may the consumption of unusual meat which might be bat or primate.

164
Q

what types of things may you see o/e VHF

A

High temperature.
Pharyngitis, conjunctival injection.
Oedema, not dependent.
Maculopapular, petechial or ecchymotic rash.
Hypotension or shock.
Haemorrhage in mucous membranes.
Jaundice - sometimes seen where there is hepatic involvement.
Oedema secondary to acute kidney injury
In advanced disease there may be altered mental state and circulatory collapse. This may be terminal.

165
Q

what would FBC/LFT/coag/others show VHF

A

FBC shows leukopenia and thrombocytopenia, although this may not be so with Lassa fever.
LFTs show elevated transaminases (in Lassa fever this predicts a high mortality).
Coagulation screen: partial thromboplastin time (PTT), INR and clotting times are all prolonged.
There may be evidence of DIC. D-dimer may be markedly elevated and fibrinogen levels low.

166
Q

diagnostic tests for VHF

A

PCRs
specific antibody tests can also be used

167
Q

Management VHF

A

Management is supportive, focusing on blood volume management, clotting and care of major organs, including heart and lungs.

168
Q

what is dengue fever? how is it spread? incubation

A

Dengue fever is a viral infection that can progress to viral haemorrhagic fever

transmitted by the Aedes aegypti mosquito
incubation period of 7 days

169
Q

disease course dengue fever?

A

Patients with dengue fever can be classified as:
- without warning signs
- with warning signs
- dengue haemorrhagic fever

‘warning signs’ include:
abdominal pain
hepatomegaly
persistent vomiting
clinical fluid accumulation (ascites, pleural effusion)

170
Q

Presentation dengue fever

A

fever
headache (often retro-orbital)
myalgia, bone pain and arthralgia (‘break-bone fever’)
pleuritic pain
facial flushing (dengue)
maculopapular rash
haemorrhagic manifestations e.g. positive tourniquet test, petechiae, purpura/ecchymosis, epistaxis

‘warning signs’ include:
abdominal pain
hepatomegaly
persistent vomiting
clinical fluid accumulation (ascites, pleural effusion)

171
Q

what are the classical features of dengue

A

Retro-orbital headache
facial flushing
bone pain and arthralgia (‘break-bone fever’)

172
Q

what is dengue haemorrhagic fever

A

Severe dengue (dengue haemorrhagic fever)
this is a form of disseminated intravascular coagulation (DIC) resulting in:
thrombocytopenia
spontaneous bleeding
around 20-30% of these patients go on to develop dengue shock syndrome (DSS)

173
Q

plan ?dengue

A

bloods-
leukopenia, thrombocytopenia, raised aminotransferases

diagnostic tests
serology
nucleic acid amplification tests for viral RNA
NS1 antigen test

Treatment
entirely symptomatic e.g. fluid resuscitation, blood transfusion etc
no antivirals are currently available

174
Q

what is yellow fever? how is ot spread? incubation?

A

Type of viral haemorrhagic fever
zoonotic infection: spread by Aedes mosquitos
incubation period = 2 - 14 days

175
Q

presentation yellow fever

A

classic description involves : 1. sudden onset of high fever, rigors, nausea & vomiting. Bradycardia may develop.
2. A brief remission is followed by jaundice, haematemesis, oliguria
if severe jaundice, haematemesis may occur

176
Q

How is ebola spread?

A

human-to-human transmission via direct contact (through broken skin or mucous membranes) with the blood, secretions, organs or other bodily fluids of infected people, and with surfaces and materials (e.g. bedding, clothing) contaminated with these fluids.

177
Q

what is ebola ? spread? incubation?

A

VHF

human-human transmission

incubation 2-21 days

178
Q

when should you suspect ebola in particualr?

A

Ebola should be suspected in patients presenting to primary care services who have a fever of 37.5°C OR have a history of fever in the past 24 hours AND have recently visited any of the affected areas (see maps) within the previous 21 days
OR
Have a fever of 37.5°C OR have a history of fever in the past 24 hours AND have cared for/come into contact with body fluids of/handled clinical specimens (blood, urine, faeces, tissues, laboratory cultures) from an individual or laboratory animal known or strongly suspected to have VHF.

179
Q

what are enteric fevers?

A

Typhoid and paratyphoid are caused by Salmonella typhi and Salmonella paratyphi (types A, B & C) respectively.

They are often termed enteric fevers, producing systemic symptoms such as headache, fever, arthralgia.

unlike other members of sanmolnella group, they more commonly cause constipation, rather than diarrhoea

180
Q

Presentation enteric fevers

A

systemic upset
relative bradycardia
abdominal pain
distension
constipation
rose spots (erythematous rash on her trunk and back ) : present on the trunk in 40% of patients, and are more common in paratyphoid

181
Q

complications enteric fevers

A

osteomyelitis (especially in sickle cell disease where Salmonella is one of the most common pathogens)
GI bleed/perforation
meningitis
cholecystitis
chronic carriage (1%, more likely if adult females)

182
Q

What is Schistosomiasis

A

Schistosomiasis, or bilharzia, is a parasitic flatworm infection. The three main species of schistosome are S. mansoni, S. japonicum and S. haematobium.

183
Q

What are the different manifestations of schistosomiasis

A

Acute manifestations may include:
- swimmers’ itch
- acute schistosomiasis syndrome (Katayama fever)
- Chronic infections caused by Schistosoma haematobium

184
Q

how does acute schistosomiasis present?

A

(Katayama fever)
fever
urticaria/angioedema
arthralgia/myalgia
cough
diarrhoea
eosinophilia

185
Q

how does chronic schistosomiasis present? invetsigation?what is the pthophysiology?

A

frequency
haematuria
bladder calcification (X-RAY)

Investigation
for asymptomatic patients serum schistosome antibodies are generally preferred
for symptomatic patients the gold standard for diagnosis is urine or stool microscopy looking for eggs

These worms deposit egg clusters (pseudopapillomas) in the bladder, causing inflammation. The calcification seen on x-ray is actually calcification of the egg clusters, not the bladder itself.

Depending on the site of these pseudopapillomas in the bladder, they can cause an obstructive uropathy and kidney damage.

186
Q

management of chronic schistosomiasis

A

single oral dose of praziquantel

187
Q

What things do you need to consider when assessing someone with a human/animal bite

A
  • is the pt at risk of tetanus (soil/debris/bleeding)

-is the pt at increased risk of the wound being infected? eg type of wound, immunocompromised

  • is the pt at risk of blood borne diseases?
  • is the pt at risk of rabies?
  • is there a safe-guarding risk? DOCUMENT EVERYTHING
  • does the pt need abx (broken skin and drawn blood)
188
Q

what things do you look for when examining a bite wound

A

The location of the wound. Photographs or diagrams may be useful.
The size, extent, and depth of the injury.
The type of wound (for example laceration, puncture, abrasion, crush, haematoma, avulsion, or amputation).
The degree of crush injury, devitalized tissue, nerve or tendon damage, and involvement of muscle, bones, joints, or blood vessels.
Examine wounds overlying a joint through the full range of motion to detect retracted injuries and tendon rupture.
Neurovascular function in the area distal to the bite — check pulses and sensation.
The range and movement of any adjacent joints.
Any lymphadenopathy.
The presence of any foreign bodies (for example teeth) in the wound.
Any signs of infection (for example redness, swelling, induration, necrotic tissue, purulent discharge, pain, localized cellulitis, lymphangitis, lymphadenopathy, or fever).
Facial bites: perform an intraoral examination to exclude cheek lacerations with an intraoral communication.

189
Q

what factors make a bite a ‘tetanus prone’ wound

A

A need for surgical intervention which is delayed for more than 6 hours.
A significant amount of devitalized tissue
A puncture wound (especially if in contact with soil or manure).
Contamination with material likely to contain tetanus spores, such as soil or manure.
A foreign body in the wound.
A compound fracture.
Systemic sepsis.

190
Q

how to manage a tetanus prone wound?

A

use ‘green book’ tetanus guidance

if full childhood imms but > 10 yr ago, req tetanus booster vaccine (+ if HIGH RISK give TIG)

if incomplete childhood imms - tetanus vaccine plus IM TIG

TIG is tetanus immunoglobulin IM

191
Q

initial wound management bite wound

A

If possible remove any foreign bodies (for example, teeth) from the wound.
Encourage the wound to bleed (if it has just occurred), unless it is already bleeding freely.
Irrigate thoroughly with warm, running water or normal saline. It is usually not possible to irrigate small puncture wounds.
Consider the need for debridement (for example, if the wound is dirty or there is non-viable tissue) and refer to Accident and Emergency if this is required and the skills and resources are not available in primary care.
Advise analgesia (paracetamol or ibuprofen) for pain relief, if required.
Where body tissue has been torn off as a result of a bite, wrap any torn-off parts (for example, part of an ear) in clean tissue and store in a plastic bag surrounded by ice for transport to hospital.
Cover the wound with an appropriate clean dressing.

192
Q

when do you offer abx for a bite? which abx?

A

Offer abx if a bite has broken the skin and drawn blood or if it is a deep cat bite that hasn’t drawn blood

co-amoxiclav for 3 days

For adults and young people aged 12 to 17 years, prescribe metronidazole plus doxycycline for 3 days.
For children aged under 12 years, prescribe co-trimoxazole for 3 days.

193
Q

How to assess rabies risk in a person with an animal bite

A

UKHSA Rabies post exposure risk assessment form and calendar

194
Q

what kind of infection do human bites cause

A

Human bites commonly cause multimicrobial infection, including both aerobic and anaerobic bacteria.

Common organisms include:
Streptococci spp.
Staphylococcus aureus
Eikenella
Fusobacterium
Prevotella

195
Q

how to assess and manage risk of blood borne infections following human bite

A
  • find out as much infor about pt and biter - any known status’, vaccination history
  • both biter and bitten person are at risk (biter even more so)
  • Offer to test for Hepatitis B, Hepatitis C, and HIV
  • At time of incident, send 10ml clotted blood for storage
  • 6w later send :
    Hep B - HbsAg
    Hep C PCR
    HIV Ag/Ab combined test
  • at 3 and 6 mo send:
    Hep B - HbsAg
    Hep C Ab
    HIV Ag/Ab combined test
196
Q

what causes cat scratch disease

A

Gram negative rod Bartonella Henselae

Cats become infected with Bartonella henselae from the bites of infected fleas or contact with infected blood

197
Q

features of cat scratch disease

A

fever
History of cat scratch
Regional Lymphadenopathy
Headache, malaise

  • one or more erythematous lesions at the site of inoculation, 3-12 days after scratch from a cat - most likely a kitten with fleas
  • O/e: crusted papeles or, rarely, a pustule
  • 1-3 weeks after primary lesion, regional lymphadenopathy appears, usually next to innoculation site - painful and may suppurate
  • Systemic symptoms: fever malaise, headache, anorexia
198
Q

complications cat scratch

A

aseptic meningitis
Encephalopathy
Prolonged fever
Myelitis, paraplegia, cerebral arthritis
Joint pain
Back pain
If innoculation directly into eye —> unilateral granulomatous conjunctivitis
Neuroretinitis
Abdominal pain (hepatitis/splenitis)

199
Q

management cat scratch disease

A

supportice - antipyretics and analgesia

may need fluctulant tender nodes aspirated

Antibiotics are indicated in immunocompromised patients and atypical cases involving severe or systemic disease. Trimethoprim-sulfamethoxazole, ciprofloxacin or azithromycin are used first-line, with gentamicin being reserved for the severely ill patient.
Patients should follow up in 2-6 months for confirmation of symptom resolution.

200
Q

prevention of cat scratch disease

A

Vigilant elimination of fleas from cats.[12]
Avoiding traumatic injury from cats, especially kittens. Cat-scratches and bites should be washed immediately and cats should not be allowed to lick open wounds

201
Q

what are the stages of lyme disease

A

Stage 1: inoculation and localised infection
PC; erythema migrans

Stage 2: dissemination
joints, heart, nervous system
PC: flu-like illness, headache, feve, tiredness, n&v
PC: facial nerve palsy, meningitis, encephalitis, peripheral mononeuritis
PC: migratory joint pain
PC: carditis with heartblock

Stage 3: late manifestations/ dysregualted host immune response
PC: chronic arthritis, encephalopathy or peripheral neuropathy, ‘post-Lyme syndrome’

202
Q

what is lyme disease? causative organism?

A

transmitted by bite of infected Ixodes ticks

The risk of transmission increases with the duration of tick attachment, with the highest risk occurring after 36-48 hours.

Lyme disease is caused by the spirochete bacterium Borrelia burgdorferi,

203
Q

investigations lyme disease

A

If considering testing for Lyme disease, speak to ID

Erythema migrans and a history of tick bite or likely exposure
Treat with oral abx for 2-3 weeks. DO NOT TEST

Discuss any other cases with ID
If high clinical suspicion - investigate but start treatment before results

  1. ELIZA
  2. Immunoblot
204
Q

management lyme disease

A

Doxycycline 100 mg bd or amoxicillin 500 mg tds.

Cefuroxime 500 mg bd if both are contra-indicated and there is no history of anaphylaxis with penicillins.

205
Q

what is leptosporosis

A

Zoonotic disease (animal —> human)
Caused by spirochaetes of the genus leptospira
In humans, the infection most commonly comes from rats

Disease is acquired through contact with contaminated water or soil, or through contact with urine or tissues of infected animals.
Leptospires enter the bloodstream through abraded skin, mucosal membranes or conjunctiva from contaminated water or soil.

206
Q

features of leptosporosis

A

Infection occurs as two syndromes: anicteric (which is self-limiting, and may present as a flu-like illness) and icteric leptospirosis (a potentially severe condition also known as Weil’s disease)

fever
Flu-like symptoms
Renal failure
Jaundice
Subconjunctival haemorrhage
Headache —> meningitis

“one-week history of fever and flu-like symptoms. On examination, there is hepatomegaly, red conjunctiva and he is jaundiced. Bloods reveal an acute kidney injury and deranged liver function tests.”

207
Q

risk factors for leptosporosis

A

Occupational: farmers, vets, abattoir, rodent control workers, butchers, SEWAGE WORKERS, septic tank workers, rice field workers, flood relief,

Recreational: open water swimming, water sports,

208
Q

management weils disease

A

High dose benzoyl-penicillin or doxycycline
Supportive care

209
Q

what is anthrax

A

Caused by the gram positive spore-forming bacterium bacillus anthracis

Spores can remain dormant in soil for decades
The disease occurs most often in wild and domestic animals in Asia, Africa and parts of Europe. Humans generally acquire the disease through infected animals or contaminated animal products

210
Q

what are the different forms of anthrax disease

A

Cutaneous (from touching a dead animal or animal tanning business for example)
inflamed itchy pimple —> vesicle —> ulcerates
Contact with skin lesions can transmit cutaneous infection

Inhalation
Pulmonary anthrax: flu-like, nausea, vomiting, sore throat, cough, sweats,fever, confusion, headache and myalgia. Patients also develop pallor or cyanosis, dyspnoea, tachycardia, abdominal pain and pleuritic chest pain

211
Q

What to do if you suspect anthrax

A

call ID and infection control

TREAT IF CLINICAL SUSPICION. HIGH MORTALITY IF DELAYED

60 days of 3 abx

continually review resp support need - can deteriorate v quickly

212
Q

what is botulism

A

Botulism is caused by botulinum toxin which is a poison produced by the obligate anaerobic bacteria Clostridium botulinum, Clostridium baratii and Clostridium butyricum.

The organism is common in the soil and can survive in this environment in the form of a resistant spore.

213
Q

what are the two main forms of botulism

A

food botulism - airtight container, uncooked food

wound botulism - IVDU

214
Q

presentation botulism

A

Acute symmetrical, descending, flaccid paralysis

blurred vision.
difficulty in swallowing and speaking.
diarrhoea and vomiting.
descending weakness or paralysis, that may extend to complete flaccid paralysis.
The patient remains alert.

215
Q

clinical signs botulism

A

Acute onset of bilateral cranial nerve involvement.
Failure of accommodation.
Pupils fixed in mid position or dilated.
Fever is unusual, as is loss of sensation

216
Q

management of botulism

A

resp support

anti-toxin

217
Q
A

Core clinical problems (94 decks)

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